GH REPLACEMENT FAILS TO IMPROVE VENTRICULAR-FUNCTION IN HYPOPHYSECTOMIZED RATS WITH MYOCARDIAL-INFARCTION

To determine whether growth hormone (GH) replacement improves cardiac function, GH-deficient hypophysectomized rats with moderate myocardial infarction (MI) were studied after 3 wk of treatment with either reco mbinant rat GH (3.2 mg . kg(-1). day(-1) sc) or vehicle. The serum ins ulin-like growth factor I level in rats after GH treatment was similar to 10-fold greater than in vehicle-treated rats. GH replacement preve nted a decrease in body weight at 1 wk (+5 +/- 6 vs. -26 +/- 4 g in ve hicle group, P < 0.01) and increased body weight at 3 wk (+40 +/- 5 vs . -30 +/- 4 g in vehicle group, P < 0.01) after MI. Infarct size, expr essed as a percentage of left ventricular (LV) perimeter, was similar for GH-treated (21 +/- 3%) and vehicle-treated (23 +/- 3%) rats. Basal LV systolic pressure, LV end-diastolic pressure, LV dP/dt, mean arter ial pressure and heart rate, and the changes in these parameters in re sponse to isoproterenol and norepinephrine were similar for these two groups. Although GH replacement tended to prevent depression in myocar dial contractility during the recovery period after maximal stimulatio n either by the largest dose of isoproterenol (0.8 mu g/kg iv) or by a cute volume loading, differences between the two groups were not stati stically significant. In addition, to determine the effects of excess CH treatment in a severe state of cardiac dysfunction, nonhypophysecto mized rats with larger infarcts (i.e., >45% of the LV) were studied af ter 4 wk of treatment. There were no differences either in hemodynamic indexes or in infarct size between the GH- and vehicle-treated groups , whereas body weight had increased (P ( 0.01) in the GH-treated group . Thus, although GH treatment effectively prevents the loss of body we ight after MI, neither GH replacement nor excess GH treatment plays an important role in preserving cardiac function in rats with moderate o r large MI.